title: Effect of metabolic abnormalities on endothelial dysfunction in normotensive offspring of subject with hypertension.
abstract: OBJECTIVE
  Essential hypertension (EH) is often accompanied by hyperinsulinemia/insulin resistance (IR) and deranged adiponectin secretion. IR may in turn be associated with endothelial dysfunction and increased levels of asymmetric dimethylarginine (ADMA). Therefore, we aimed to determine metabolic abnormalities in normotensive offspring of subjects with essential hypertension (familial trait-FT) and to examine their relations to endothelium-dependent vasodilation of the brachial artery (BA).
  
  
  METHODS
  We included 77 subjects, 38 were normotensive individuals with FT aged 28-39 (mean 33) years and 39 age-matched Controls without FT. Insulin, adiponectin and ADMA plasma levels were determined by radioimmunoassay. Using high-resolution ultrasound, BA diameters at rest and during reactive hyperemia (flow-mediated dilation-FMD) were measured.
  
  
  RESULTS
  Subjects with FT had higher insulin and lower adiponectin levels than controls (13.65±6.70 vs. 7.09±2.20 mE/L; P<0.001 and 13.60±5.98 vs. 17.27±7.17 mg/L respectively; P<0.05). Insulin and adiponectin levels were negatively interrelated (r=-0.33, P=0.003). ADMA levels were comparable in both groups. The study group had worse FMD than Controls (6.11±3.28 vs. 10.20±2.07%; P<0.001). IR was independently associated with FMD (partial R2=0.23, P<0.001).
  
  
  CONCLUSIONS
  Increased insulin and decreased adiponectin levels along with endothelial dysfunction are present in normotensive subjects with FT. IR and hypoadiponectinemia are interrelated, but only hyperinsulinemia has an independent adverse influence on endothelial function. Results of our study did not confirm the role of ADMA in pathogenesis of evolving hypertension.
authors.affiliation: Department of Vascular Diseases, University Medical Centre Ljubljana, Ljubljana, Slovenia. drzizek@hotmail.com
authors.forename: B
authors.initials: B
authors.lastname: Žižek
authors.forename: D
authors.initials: D
authors.lastname: Žižek
authors.forename: K
authors.initials: K
authors.lastname: Bedenčič
authors.forename: A
authors.initials: A
authors.lastname: Jerin
authors.forename: P
authors.initials: P
authors.lastname: Poredoš
mesh_terms: D052242:Adiponectin / Q000097:blood; D000328:Adult; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D015415:Biomarkers / Q000097:blood; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D020022:Genetic Predisposition to Disease; D040941:Heredity; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D006946:Hyperinsulinism / Q000097:blood / Q000235:genetics* / Q000503:physiopathology; D006973:Hypertension / Q000097:blood / Q000235:genetics* / Q000503:physiopathology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance / Q000235:genetics*; D016014:Linear Models; D008297:Male; D015999:Multivariate Analysis; D010375:Pedigree; D010641:Phenotype; D012307:Risk Factors; D014463:Ultrasonography; D014664:Vasodilation / Q000235:genetics*
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D007328:Insulin; C018524:N,N-dimethylarginine; D001120:Arginine